To test the validity of the ASTEROID stereotest as a clinical test of depth perception by comparing it to clinical and research standard tests.
Thirty-nine subjects completed four stereotests twice the ASTEROID test on an autostereo 3D tablet, a research standard on a VPixx PROPixx 3D projector, Randot Circles, and Randot Preschool. Within 14 days, subjects completed each test for a third time.
ASTEROID stereo thresholds correlated well with research standard thresholds (= 0.87, &lt; 0.001), although ASTEROID underestimated standard threshold (mean difference = 11 arcsec). ASTEROID results correlated less strongly with Randot Circles (= 0.54, &lt; 0.001) and Randot Preschool (= 0.64, &lt; 0.001), due to the greater measurement range of ASTEROID (1-1000 arcsec) compared to Randot Circles or Randot Preschool. Stereo threshold variability was low for all three clinical stereotests (Bland-Altman 95% limits of agreement between test and retest ASTEROID, ±0.37; Randot Circles, ±0.24; Randot Preschool, ±0.23). ASTEROID captured the largest range of stereo in a normal population with test-retest reliability comparable to research standards (immediate = 0.86 for ASTEROID vs. 0.90 for PROPixx; follow-up = 0.68 for ASTEROID vs. 0.88 for PROPixx).
Compared to clinical and research standards for assessing depth perception, ASTEROID is highly accurate, has good test-retest reliability, and measures a wider range of stereo threshold.
The ASTEROID stereotest is a better clinical tool for determining baseline stereopsis and tracking changes during treatment for amblyopia and strabismus compared to current clinical tests.
The ASTEROID stereotest is a better clinical tool for determining baseline stereopsis and tracking changes during treatment for amblyopia and strabismus compared to current clinical tests.To validate the application of a known transgenic mouse line with green fluorescent cones (Chrnb4.EGFP) to study cone photoreceptor biology and function in health and disease.
Chrnb4.EGFP retinas containing GFPcones were compared with retinas without the GFP transgene via immunohistochemistry, quantitative real-time polymerase chain reaction, electroretinograms, and flow cytometry. The Chrnb4.EGFP line was backcrossed to the mouse models of cone degeneration, and , generating the new lines .GFP and .GFP, which were also studied as described.
GFP expression spanned the length of the cone cell in the Chrnb4.EGFP line, as well as in the novel .GFP and .GFP lines. The effect of GFP expression showed no significant changes to outer nuclear layer cell death, cone-specific gene expression, and immune response activation. A temporal decrease in GFP expression over time was observed, but GFP fluorescence was still detected through flow cytometry as late as 6 months. Furthermore, a functional analysis of photopic and scotopic electroretinogram responses of the Chrnb4 mouse showed no significant difference between GFPand GFPmice, whereas electroretinogram recordings for the .GFP and .GFP lines matched previous reports from the original lines.
This study demonstrates that the Chrnb4.EGFP mouse can be a powerful tool to overcome the limitations of studying cone biology, including the use of this line to study different types of cone degeneration.
This work validates research tools that could potentially offer more reliable preclinical data in the development of treatments for cone-mediated vision loss conditions, shortening the gap to clinical translation.
This work validates research tools that could potentially offer more reliable preclinical data in the development of treatments for cone-mediated vision loss conditions, shortening the gap to clinical translation.High circulating levels of the hormone prolactin (PRL) protect against experimental diabetic retinopathy (DR) due to the retinal accumulation of vasoinhibin, a PRL fragment that inhibits blood vessel permeability and growth. A phase 2 clinical trial is investigating a new therapy for DR based on elevating serum PRL levels with levosulpiride, a prokinetic dopamine D2 receptor blocker. Here, we tested whether levosulpiride-induced hyperprolactinemia elevates PRL and vasoinhibin in the vitreous of volunteer patients with proliferative DR (PDR) undergoing elective pars plana vitrectomy.
Patients were randomized to receive placebo (lactose pill, orally TID; = 19) or levosulpiride (25 mg orally TID; = 18) for the 7 days before vitrectomy. Vitreous samples from untreated non-diabetic (= 10) and PDR (= 17) patients were also studied.
Levosulpiride elevated the systemic (101 ± 13 [SEM] vs. 9.2 ± 1.3 ng/mL, &lt; 0.0001) and vitreous (3.2 ± 0.4 vs. https://www.selleckchem.com/products/bay-985.html 1.5 ± 0.2 ng/mL, &lt; 0.0001) levels of PRL, and both levels were directly correlated (= 0.58, &lt; 0.0002). The vitreous from non-diabetic patients or from PDR patients treated with levosulpiride, but not from placebo-treated PDR patients, inhibited the basic fibroblast growth factor (bFGF)- and vascular endothelial growth factor (VEGF)-induced proliferation of endothelial cells in culture. Vasoinhibin-neutralizing antibodies reduced the vitreous antiangiogenic effect. Matrix metalloproteases (MMPs) in the vitreous cleaved PRL to vasoinhibin, and their activity was higher in non-diabetic than in PDR patients.
Levosulpiride increases the levels of PRL in the vitreous of PDR patients and promotes its MMP-mediated conversion to vasoinhibin, which can inhibit angiogenesis in DR.
These findings support the potential therapeutic benefit of levosulpiride against vision loss in diabetes.
These findings support the potential therapeutic benefit of levosulpiride against vision loss in diabetes.To compare electrophysiological and pupillometric responses in subjects with cone-rod dystrophy due to autosomal recessive (AR) mutations.
Four subjects with AR dystrophy and 10 visually normal, age-similar controls participated in this study. Full-field, light- and dark-adapted electroretinograms (ERGs) were obtained using conventional techniques. Full-field, light- and dark-adapted measures of the pupillary light reflex (PLR; pupil constriction elicited by a flash of light) were obtained across a range of stimulus luminance using long- and short-wavelength light. Pupil size as a function of stimulus luminance was described using Naka-Rushton functions to derive (maximum response) and (pupil response sensitivity).
Light-adapted ERGs were non-detectable in all four subjects, whereas dark-adapted ERGs were non-detectable in three subjects and markedly attenuated in the fourth. By contrast, each subject had light- and dark-adapted PLRs. ranged from normal to slightly attenuated under all conditions.